Altered plasma proteins released from platelets and endothelial cells are associated with human patent ductus arteriosus.

摘要: Patent ductus arteriosus is the third most common congenital heart disease and resulted from persistence of ductal patency after birth. Ductus closure involves functional structural remodeling, controlled by many factors. The changes in plasma protein levels associated with PDA are not known. Here we for first time demonstrate six key differential proteins human patent patients using proteomic technology present a model to illustrate constriction arteriosus. Differentially expressed were analyzed isobaric tags relative absolute quantification validated enzyme-linked immunosorbent assay new samples. data have been deposited ProteomeXchange Consortium via PRIDE partner repository set identifier PXD008568. We found 74 upregulated 98 downregulated PDA. Five decreased (platelet factor 4, fibrinogen, von Willebrand factor, collagen, mannose binding lectin-associated serine protease-2) one increased (fibronectin) may increase risk Those closely related platelet activation coagulation cascades, complement mannan-binding-lectin, other systemic signaling pathways. Our findings indicate that involved different pathways play roles nonclosure humans be developed as biomarkers diagnosis. All those served basis understanding etiology pathogenesis